Author/Authors :
Seung-Hee Lee، نويسنده , , Chae-Seok Lim، نويسنده , , Hyungju Park، نويسنده , , Jin-A Lee، نويسنده , , Jin-Hee Han، نويسنده , , Hyoung Kim، نويسنده , , Ye-Hwang Cheang، نويسنده , , Sue Hyun Lee، نويسنده , , Yong-Seok Lee، نويسنده , , Hyoung-Gon Ko، نويسنده , , Dong-Hyuk Jang، نويسنده , , Hyongkyu Kim، نويسنده , , Maria C. Miniaci، نويسنده , , Dusan Bartsch، نويسنده , , Eunjoon Kim، نويسنده , , Craig H. Bailey، نويسنده , , Eric R. Kandel، نويسنده , , Bong-Kiun Kaang، نويسنده ,
Abstract :
Repeated pulses of serotonin (5-HT) induce long-term facilitation (LTF) of the synapses between sensory and motor neurons of the gill-withdrawal reflex in Aplysia. To explore how apCAM downregulation at the plasma membrane and CREB-mediated transcription in the nucleus, both of which are required for the formation of LTF, might relate to each other, we cloned an apCAM-associated protein (CAMAP) by yeast two-hybrid screening. We found that 5-HT signaling at the synapse activates PKA which in turn phosphorylates CAMAP to induce the dissociation of CAMAP from apCAM and the subsequent translocation of CAMAP into the nucleus of sensory neurons. In the nucleus, CAMAP acts as a transcriptional coactivator for CREB1 and is essential for the activation of ApC/EBP required for the initiation of LTF. Combined, our data suggest that CAMAP is a retrograde signaling component that translocates from activated synapses to the nucleus during synapse-specific LTF.
